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These data suggest that hADSC-ex specifically enter microglia/macrophages and suppress their activation during brain injury, thereby inhibiting inflammation and facilitating functional recovery. They also offer new insight into the cellular targeting, uptake and migration of hADSC-ex, and provide a theoretical basis for new therapeutic strategies for central nervous system diseases.Inflammatory damage to endothelial cells plays a pivotal role in the diabetes-provoked atherosclerosis (AS). PYD domains-containing protein 3 (NLRP3) induces fo
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